Abstract:

Eukaryotic cells respond to various types of stresses caused by
changes in the extracellular environment. Intracellular factors, such as the
accumulation of misfolded proteins in the endoplasmic reticulum (ER), also
cause stress and activate the unfolded protein response (UPR), which induces
the expression of chaperones and proteins involved in the recovery process. However, if the stress is
excessive or sustained, and ER function cannot be restored, the UPR triggers apoptosis, thereby removing the
affected cell. It is now apparent that ER stress is also a potent trigger for autophagy, a self-degradative
process that has an adaptive function. This review surveys the intersection of ER stress and autophagy and
highlights the potential therapeutic implications thereof.

Abstract:Eukaryotic cells respond to various types of stresses caused by
changes in the extracellular environment. Intracellular factors, such as the
accumulation of misfolded proteins in the endoplasmic reticulum (ER), also
cause stress and activate the unfolded protein response (UPR), which induces
the expression of chaperones and proteins involved in the recovery process. However, if the stress is
excessive or sustained, and ER function cannot be restored, the UPR triggers apoptosis, thereby removing the
affected cell. It is now apparent that ER stress is also a potent trigger for autophagy, a self-degradative
process that has an adaptive function. This review surveys the intersection of ER stress and autophagy and
highlights the potential therapeutic implications thereof.